FIGURE 7.

Proposed substrate carbon flow through the truncated Krebs/TCA cycle of tumor mitochondria. Cholesterol-rich tumor mitochondria preferentially export pyruvate-generated citrate as the primary source of cytosolic acetyl-CoA to support the tumor’s enhanced cholesterogenesis, rather than utilize it as substrate for oxidative phosphorylation. Nevertheless, cholesterol-rich tumor mitochondria efficiently engage mitochondrial respiration when fueled, for example, with glutamate together with the malate re-entering in exchange for exiting citrate on the CTP (see text for further details).